Bahloul Mabrouk, Bouchaala Karama, Chtara Kamilia, Kharrat Sana, Bouaziz Mounir
Department of Intensive Care, Habib Bourguiba University Hospital, Sfax University, Sfax, Tunisia.
Am J Trop Med Hyg. 2024 Oct 8;111(6):1178-1183. doi: 10.4269/ajtmh.24-0163. Print 2024 Dec 4.
Myocardial ischemia after severe scorpion envenomation is rarely reported. The aim of this review was to elaborate on a review of myocardial ischemia after severe scorpion envenomation and to detail the mechanism of this myocardial hypoperfusion. We used the PubMed database and entered the following keywords in MeSH research: scorpion envenomation, myocardial ischemia, myocardial perfusion scintigraphy, echocardiography, and troponins. The literature analysis confirmed that severe scorpion envenomation can be complicated by temporary myocardial ischemia, based on electrocardiographic, histopathologic, echocardiographic, myocardial perfusion scintigraphy, and biological studies. The correlation between clinical manifestations, laboratory and electrocardiographic evidence of myocardial damage, echocardiographic studies, perfusion scintigraphy abnormalities, and histopathologic findings are suggestive of lesions of cardiac fibers secondary to myocardial ischemia. Myocardial hypoperfusion may be due to multiple factors. First, catecholamine storms can induce microvascular constriction. On the other hand, the release of catecholamines through a complex neurohormonal interaction with other neuropeptides and cytokine release can produce/induce major coronary microvascular constriction and/or microvascular injury, leading to microvascular acute coronary syndrome with Takotsubo cardiomyopathy. The management of severe scorpion envenomation with severe myocardial failure and pulmonary edema is based on oxygen with invasive or noninvasive ventilator support. Dobutamine improves cardiac function after scorpion envenomation. Antiplatelet therapy is not recommended. In conclusion, severe scorpion envenomation can be complicated by temporary myocardial ischemia, which can be due to multiple factors.
严重蝎螫伤后发生心肌缺血的情况鲜有报道。本综述的目的是详细阐述严重蝎螫伤后心肌缺血的相关情况，并详述这种心肌灌注不足的机制。我们使用了PubMed数据库，并在医学主题词（MeSH）检索中输入了以下关键词：蝎螫伤、心肌缺血、心肌灌注闪烁显像、超声心动图和肌钙蛋白。文献分析证实，基于心电图、组织病理学、超声心动图、心肌灌注闪烁显像及生物学研究，严重蝎螫伤可并发暂时性心肌缺血。临床表现、心肌损伤的实验室及心电图证据、超声心动图研究、灌注闪烁显像异常及组织病理学发现之间的相关性提示，心肌缺血继发心脏纤维病变。心肌灌注不足可能由多种因素导致。首先，儿茶酚胺风暴可诱发微血管收缩。另一方面，通过与其他神经肽及细胞因子释放的复杂神经激素相互作用释放儿茶酚胺，可导致/诱发主要冠状动脉微血管收缩和/或微血管损伤，进而引发伴有Takotsubo心肌病的微血管急性冠状动脉综合征。对于伴有严重心肌衰竭和肺水肿的严重蝎螫伤患者，治疗措施包括使用有创或无创呼吸机支持给氧。多巴酚丁胺可改善蝎螫伤后的心脏功能。不建议使用抗血小板治疗。总之，严重蝎螫伤可并发暂时性心肌缺血，其原因可能是多方面的。
